Aim of the study: To investigate the effects of shikonin on CD36 expression and phagocytic ability of microglia, and its protective effect on neurons and the possible mechanism within.
Material and methods: The effects of shikonin on CD36 expression and phagocytic ability of microglia were detected by Western blot method, and cerebral haemorrhage was isolated by flow cytometry in the experiment. The protective effect of neurons was observed through neuron-microglia co-culture technique. Meanwhile, the effect of hydrogen peroxide on the expression of catalase was detected, and the concentration of hydrogen peroxide was measured in the isolated cerebral haemorrhage model. The t test was used to compare data between 2 groups, and one-way ANOVA was applied to multiple sets of data.
Results: Compared with the control group, the CD36 expression and phagocytic ability of microglia was increased by shikonin in the isolated cerebral haemorrhage model, while inflammatory factors such as tumour necrosis factor a (TNF-a) and interleukin 1b (IL-1b) attenuated the effects of the drug. The amount of neuron apoptosis/necrosis was significantly reduced by the drug, while the expression of catalase in microglia was increased, but the secretion of hydrogen peroxide was decreased in the neuron-microglia co-culture system.
Conclusions: Shikonin can enhance the CD36 expression and the ability to phagocytose erythrocyte of microglia. Simultaneously, shikonin performs protective effects on neuronal cells and promotes the absorption of haematoma. Therefore, shikonin is probably an innovative medicine to treat cerebral haemorrhage.
Keywords: TLR4 signalling pathway.; cerebral haemorrhage; haematoma absorption; inflammation; CD36.